Subnormal platelet response to thromboxane A2 in a patient with chronic myeloid leukaemia.
A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin-induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (greater than or equal to 2 mM) induced minimal reversible aggregation. 14C-serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin-layer radiochromatographic analysis of the metabolites of 14C-AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet-rich plasma was added to a reaction mixture in which thromboxane A2 (TXA2) had been generated. TXA2 produced by patient's platelets showed normal platelet-aggregating activity. These results suggest that a subnormal platelet response to TXA2 is included as a mechanism for this acquired hypofunction of the platelet.
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001791:Blood Platelet Disorders / Q000209:etiology*; D001792:Blood Platelets / Q000378:metabolism; D005260:Female; D006801:Humans; D007951:Leukemia, Myeloid / Q000097:blood / Q000150:complications*; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010979:Platelet Function Tests; D013928:Thromboxane A2 / Q000494:pharmacology*; D013931:Thromboxanes / Q000494:pharmacology*
D001095:Arachidonic Acids; D013931:Thromboxanes; D016718:Arachidonic Acid; D013928:Thromboxane A2; D000255:Adenosine Triphosphate